| 摘要 |
The original abstract exceeded 150 words in length. As a result, the abstract has been established as follows: Disclosed are methods for treating a tumor, specifically breast tumors. Increased mitochondrial "power" in epithelial cancer cells oncogenically promotes tumor growth, by conferring autophagy-resistance. As such, PGC-1 alph, PGC-1 beta, mitoNEET, and POLRMT should all be considered as tumor promoters or "metabolic oncogenes". Our results are consistent with numerous previous clinical studies showing that metformin (a weak mitochondrial "poison") prevents the onset of nearly all types of human cancers in diabetic patients. Metformin (a Complex I inhibitor), and other mitochondrial inhibitors, are disclosed as novel anti-cancer therapies, targeting mitochondrial metabolism in cancer cells. |
